Biomedical subjects

C K Joo

Publications and source records attributed to C K Joo.

At least 19 recordsLinked to original sources

PubMed2001

Overexpression of matrix metalloproteinase-2 mediates phenotypic transformation of lens epithelial cells.

Transforming growth factor-beta (TGF-beta) is known to be a causative factor in pathological fibrosis and the metastasis of cancer cells, through effects on molecules of the extracellular matrix (ECM). We evaluated the influence of TGF-beta(1) on the gene expression of matrix metalloproteinase-2 (MMP-2) in lens epithelial cells (LECs). The results showed that TGF-beta(1) induced the expression of mRNA for MMP-2 in LECs. Subsequently, in order to examine the role of MMP-2, we overexpressed MMP-2 in LECs by stable transfection. The MMP-2-overexpressing LECs showed typical indicators of a myofibroblast-like cell phenotype, such as multiple layers of cells, elongated morphology, and expression of alpha-smooth muscle actin. We also showed that an MMP inhibitor blocked the TGF-beta(1)-induced morphological change in LECs. These results demonstrate that MMP-2 plays a role in the transformation of LECs, which has implications for the pathological fibrosis of these cells.

Animals↗

PubMed2001

Hydrogen peroxide is a novel inducer of connective tissue growth factor.

Connective tissue growth factor (CTGF) has recently been described as a fibrogenic factor and is greatly induced by various extracellular stimuli, such as transforming growth factor-beta (TGF-beta), dexamethasone, and serotonin. CTGF induces collagen type I and fibronectin, and the deposition of such molecules leads to fibrotic disease in many tissues. Intracellular reactive oxygen species (ROS) are generated by extracellular stress conditions and are produced as by-products of cellular metabolism. Imbalanced cellular redox status is a potent pathogenic factor that leads to various degenerative diseases, including tissue fibrosis. Since CTGF is believed to play a crucial role in fibrotic disease formation in many tissues, we examined the role of ROS in CTGF gene expression in human lens epithelial cell line B3. The results showed that CTGF was induced by reactive oxygen species such as hydrogen peroxide and hydroxyl radicals. Next, we examined whether CTGF induction by ROS is via newly synthesized TGF-beta. The results showed that ROS directly induced CTGF mRNA not via the increased TGF-beta synthesis or activation. Next, we treated AG490, which is the well-known inhibitor of Janus kinase (JAK), with hydrogen peroxide. AG490 abrogated the CTGF induction by ROS in a dose-dependent manner. The results suggest that JAK-2/-3 seems to be involved in the enhanced CTGF mRNA expression by hydrogen peroxide. In this report, we present that hydrogen peroxide is a novel inducer of CTGF gene expression and that JAK-2/-3 activation seems to play a role in CTGF induction.

Amino Acid Sequence↗

PubMed2001

Downregulated expression of integrin alpha6 by transforming growth factor-beta(1) on lens epithelial cells in vitro.

Integrins represent the main cell surface receptors that mediate cell-matrix and cell-cell interactions. They play critical roles in adhesion, migration, morphogenesis, and the differentiation of several cell types. Previous studies have demonstrated that members of the fibroblast growth factor (FGF)-2, transforming growth factor (TGF)-beta(1), and insulin growth factor (IGF)-1 play important roles in lens biology. In particularly, TGF-beta(1) appears to play a key role in extracellular matrix production, cell proliferation, and cell differentiation of lens epithelial cells. In this study we investigated the effects of FGF-2, TGF-beta(1), and IGF-1 on the modulation of integrin receptors using lens epithelial cell lines (HLE B-3 and alphaTN-4) and lens explants. We found that the expression of integrin alpha6 is downregulated by TGF-beta(1), but is not responsive to FGF-2 or IGF-1. The promoter activity of the integrin alpha6 gene decreased upon TGF-beta(1) treatment in a transient transfection assay, and flow cytometric analysis demonstrated the reduced expression of integrin alpha6 by TGF-beta(1), whereas significant changes were not observed in the level of integrin alpha6 after the addition of FGF-2. These findings suggest that the reduced expression of integrin alpha6 caused by TGF-beta(1) might play a role in the activation of the cell cycle genes required during the fiber differentiation of the lens.

Animals↗

PubMed2001

Attenuation of Zn2+ neurotoxicity by aspirin: role of N-type Ca2+ channel and the carboxyl acid group.

Synaptically released Zn2+ ions enter into neurons primarily through voltage-gated Ca2+ channels (VGCC) or N-methyl-d-aspartate (NMDA) receptors, which can mediate pathological neuronal death. We studied the possibility (and underlying mechanisms) that aspirin, known to prevent NMDA neurotoxicity, would also attenuate Zn2+ neurotoxicity. Administration of 3 to 10 mM aspirin, in cortical cell cultures, attenuated the evolution of neuronal death following exposure to 300 microM Zn2+ for 30 min. This neuroprotective effect of aspirin was attributable to the prevention of Zn2+ ion entry. Aspirin interfered with inward currents and an increase in [Ca2+]i through VGCC and selective binding of omega-conotoxin, sensitive to N-type Ca2+ channel. The omega-conotoxins GVIA or MVIIC, the selective inhibitors of N-type Ca2+ channels, attenuated Zn2+ neurotoxicity. Aspirin derivatives lacking the carboxyl acid group did not reduce Zn2+ neurotoxicity. The present findings suggest that aspirin prevents Zn2+-mediated neuronal death by interfering with VGCC, and its action specifically requires the carboxyl acid group.

Acetylcysteine↗

PubMed2001

Effect of a capsular tension ring on the shape of the capsular bag and opening and the intraocular lens.

PURPOSE: To evaluate the effect of a capsular tension ring (CTR) on the shape of the capsular bag, the extent of the capsular opening, and the shape of intraocular lenses (IOLs). SETTING: Department of Ophthalmology, College of Medicine, The Catholic University of Korea, Seoul, Korea. METHODS: The corneal button was removed from porcine eyes in vitro. After phacoemulsification was performed, an IOL alone or an IOL and CTR were inserted in the capsular bag in 6 groups of 5 eyes each. The eyes were examined from the posterior aspect using a Miyake technique to assess capsular bag shape and the capsular opening. To evaluate effects of the CTR on IOL shape, rabbit eyes had phacoemulsification and IOL implantation with and without placement of a CTR in vivo. The IOLs were removed from enucleated eyes 3 months postoperatively and compared with unused control IOLs. RESULTS: The differences between the maximum and minimum diameters of the capsular bags and capsular openings were significantly less in groups with a CTR. Intraocular lens size (difference from haptic to haptic) decreased significantly in eyes with only an IOL compared with normal controls or eyes with both an IOL and CTR. CONCLUSIONS: The CTR preserved the integrity of the capsular bag diameter, capsular opening, and IOL shape. It is likely that CTR implantation can avert contracture of the capsular bag and capsular opening, preventing IOL decentration.

Animals↗

PubMed2001

Expression of vascular endothelial growth factor and inducible nitric oxide synthase in pterygia.

PURPOSE: To evaluate the expression of vascular endothelial growth factor (VEGF) in pterygium and investigate the interrelationships between VEGF and nitric oxide (NO) in the development of pterygia. METHODS: Specimens of normal conjunctiva acquired incidentally to conjunctival transplantation during pterygium and strabismus surgery and the excised pterygium were used in this study. Cryopreserved tissue specimens consisting of normal conjunctiva and pterygium were used to study the expression of VEGF and inducible NO synthetase (iNOS), using immunohistochemistry. For confirmation of NOS activity, reduced nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase staining was done. Enzyme-linked immunosorbent assay (ELISA) for detection and quantification of VEGF was performed. RESULTS: Expression of VEGF and iNOS was strongly revealed mainly in the epithelium of the head portions of pterygial specimens, although not in the epithelium of conjunctival ones. Pterygial epithelium was stained with NADPH diaphorase, confirming NOS activity. ELISA showed a greater amount of VEGF in pterygium (11.7 +/- 2.1 pg/mg) compared with normal conjunctiva (4 +/- 0.47 pg/mg) ( p < 0.05). CONCLUSION: These data are the first to demonstrate that VEGF and NO may play an important role in the development of pterygium and to identify VEGF and NO in the epithelium of pterygium. We hypothesize that environmental stress, such as ultraviolet irradiation and local inflammation stimulate the elaboration of NO and VEGF, resulting in the conjunctival fibrovascular ingrowth characteristic of pterygium.

Adult↗

PubMed2001

BIGH3 gene mutations and rapid detection in Korean patients with corneal dystrophy.

PURPOSE: Mutations in the BIGH3 gene on chromosome 5q31 cause four distinct autosomal dominant corneal dystrophies. We sought to determine whether the BIGH3 gene mutation was responsible for corneal dystrophy in Korean patients. METHODS: Polymerase chain reaction single strand conformational polymorphism (PCR-SSCP) analysis was performed with the DNA from patients and healthy individuals. We sequenced the PCR products with the aberrant SSCP pattern to identify the mutation. Mutant-specific reverse primers were used to screen genomic DNA for the identified mutations. RESULTS: We identified mutations R124C in the CDL1 family and R124H in four families with a granular dystrophy. We identified our granular dystrophy to be Avellino corneal dystrophy (ACD). Eighteen of 20 patients with a granular dystrophy contained the same R124H mutation, indicating that mutation R124H was very common in Korean patients with ACD. During this study, we identified a new polymorphism (T1667C, F540F). CONCLUSIONS: This is the first report of mutations found in the BIGH3 gene in Korean families with corneal dystrophy. We report that the majority (90%) of ACD patients in Korea carry the R124H mutation. Mutant-specific reverse primers can be used to screen efficiently for CDL1 and ACD.

Adolescent↗

PubMed2001

Predictability for proper capsular tension ring size and intraocular lens size.

Predicting correct capsular tension ring size and intraocular lens size using measurements of lens diameter, corneal diameter, axial length and capsular bag diameters to determine anatomical relationships of post implantation capsular tension ring (CTR). The vertical and horizontal diameters of cornea and lens were measured in 62 human eyeballs supplied from the eye bank of the Catholic University. The relationship between corneal diameter and axial length was examined in 195 living human eyes. An extension of capsular bag diameter after implantation of CTR was measured in 19 pigs' eyes purchased from a slaughter house. The correlation between the lens diameter and the capsular bag diameter after CTR implantation was analyzed using linear regression. The average diameters (mean of horizontal and vertical diameters) of cornea and lens in human eyeball of postmortems (average age:69, ratio of male:female = 23:39) were 11.59+/-0.42 mm for horizontal diameter, 9.54+/-0.27 mm, for vertical diameter. The average corneal diameters and axial lengths in living human eyes (average age: 62, ration of male:female = 84:111) were 11.63+/-0.53 mm for the cornea diameter, 24.48+/-2.10 mm, for cornea axial length. There is a statistically significant correlation between corneal diameter and axial length (correlation coefficient=0.788; p<0.001) and corneal diameter and lens diameter (correlation coefficient=0.711; p<0.001). In pigs' eyes, there is a relationship between lens diameter and capsular bag diameter after implantation of 11 mm CTR (correlation coefficient=0.684; p<0.001). In conclusion, axial length and corneal diameter may give surgeons a valuable clue to expected size of capsular bag and important parameters for selecting the correct sized CTR and IOL.

Animals↗

PubMed2001

Central islands after LASIK detected by corneal topography.

A central island is defined as a localized elevated area in corneal topography after excimer laser application for myopic correction. We experienced 15 cases of central islands developed 1 week after LASIK using VISX STAR on corneal topography. The uncorrected visual acuity and best corrected visual acuity were 0.52 +/- 0.22, 0.66 +/- 0.25 in central islands group and 0.69 +/- 0.19, 0.78 +/- 0.19 in control group at 1 week after LASIK. The visual acuity in control group was more improved statistically significantly than central islands group (respectively p = 0.01, p = 0.03). There was no statistical significance between the two groups, although the uncorrected visual acuity and best corrected visual acuity were somewhat more increased in control group at 2 months and 6 months after LASIK than in central islands group (respectively p = 0.06, p = 0.24 at 2 months, p = 0.10, p = 0.17 at 6 months). On the changes of spherical equivalent after LASIK, both the central islands group and control group were in hyperopic state at 1 week after LASIK and were somewhat regressed to myopia at 2 months and 6 months after LASIK. But there was no statistical significance between the two groups at different time points (respectively p = 0.15, p = 0.64, p = 0.67). In 12 cases the central islands were disappeared spontaneously at 2 months, but in 3 cases the central islands were remained 6 months after LASIK on corneal topography. In the one case of 3 cases the best corrected visual acuity was 0.5 at 6 months after LASIK, but in the others the best corrected visual acuity was not different from the mean best corrected visual acuity. Most cases in LASIK, the central islands were dissapeared without specific treatments as in PRK. We suggest, in the case of central islands at 6 months after LASIK, that if the patient complain visual discomfort, monocular diplopia, haloes, or ghost images, central reablation with excimer laser should be considered.

Adult↗

PubMed2001

Complestatin is a noncompetitive peptide antagonist of N-methyl-D-aspartate and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid/kainate receptors: secure blockade of ischemic neuronal death.

Complestatin, a peptide derived from Streptomyces, was found to protect cultured cortical neurons from excitotoxicity induced by N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), or kainate. This neuroprotective behavior of complestatin was attributed to a blockade of Ca2+ ion entry and accumulation, after the activation of NMDA and AMPA/kainate receptors. Complestatin reversibly interfered with NMDA- and AMPA-mediated excitatory synaptic transmission. Complestatin also protected cortical neurons from prolonged deprivation of oxygen and glucose, more effectively than combined antagonists of NMDA and AMPA/kainate receptors. Neurotoxicity, evolving within 1 to 2 days after continuous exposure to combined NMDA and AMPA/kainate antagonists, was not observed in cortical cell cultures that were exposed to complestatin. Finally, complestatin dose dependently prevented neuronal death evolving within the inner nuclear and ganglion cell layers, after transient retinal ischemia. We conclude that complestatin possesses novel pharmacological properties that effectively prevent excitotoxicity under certain pathological conditions.

Animals↗

PubMed2000

Failure to activate NF-kappaB promotes apoptosis of retinal ganglion cells following optic nerve transection.

NF-kappaB is a transcription factor, which is activated by various stimuli. One of the well-known activators of NF-kappaB is oxidative stress, which is a cause of cell death in some tissue, or cell types. Optic nerve transection, axotomy, results in retinal cell death, because of oxidative stress, deprivation of neurotrophic factors, etc. Since it has been hypothesized that the retinal ganglion cell death after axotomy is due to the generation of reactive oxygen species, we investigated whether NF-kappaB is involved in the retinal cell death after axotomy. This study was performed to investigate the role of NF-kappaB in retinal ganglion cell death after optic nerve transection. We used double staining experiment by using anti-NF-kappaB antibody and ethidium bromide to observe the correlation of NF-kappaB activation and the cell death. NF-kappaB was observed only in the surviving cells. NF-kappaB translocation was observed 3 days after the optic nerve transection. The NF-kappaB inhibitor, sulfasalazine, was used to block the activation of NF-kappaB in the axotomized retina, and the number of ganglion cells was quantified using retrograde in the presence or absence of sulfasalazine after axotomy. Inhibition of NF-kappaB by sulfasalazine accelerated the degeneration of ganglion cells in the retina. The results suggest that the activated NF-kappaB plays a protective role from the cell death in the injured ganglion cells.

Animals↗

PubMed2000

Effect of advanced glycation end products on lens epithelial cells in vitro.

The extended exposure of proteins to reducing sugars leads to nonenzymatic glycation with the accumulation of advanced glycation end products (AGEs). Long-lived proteins, such as collagen and crystallins, are subjected to this modification, and are implicated as causal factors in several diseases including diabetic complications, cataracts, and arteriosclerosis. One means through which AGEs modulate cellular interactions is via binding to specific receptors. In the current study, the existence of AGEs in human anterior polar lens capsules of cataracts was confirmed using a combination of dot-immunoblot and fluorescent detection. Human lens epithelial cells (LECs) attached to anterior lens capsules expressed mRNA for the receptor for AGEs (RAGE). The interaction of LECs with AGEs using bovine lens epithelial explants demonstrated that AGEs induced mRNAs and proteins of fibronectin, collagen type I, aberrant extracellular matrix proteins, and alpha-SMA, a specific marker for myofibroblastic cells. These findings suggest that AGEs may alter cellular functions which induce mRNAs and proteins associated with fibrosis in LECs.

Actins↗

PubMed2000

Repopulation of denuded murine Descemet's membrane with life-extended murine corneal endothelial cells as a model for corneal cell transplantation.

BACKGROUND: Corneal endothelial cell transplantation has been an intriguing concept as an alternative to full-thickness penetrating keratoplasty. Using a murine corneal transplantation model, we sought to establish the optimal conditions to repopulate, ex vivo, denuded murine Descemet's membrane with life-extended cell cultures of murine corneal endothelial cells. These ex vivo repopulated corneas were used as donor corneas in a murine orthotopic corneal transplantation model to assess, in vivo, the function of the transplanted, life-extended murine corneal endothelial cells (MCEC). METHODS: Mouse corneas were surgically trephined and the native corneal endothelium was removed mechanically using a sterile cotton swab. Cultured murine corneal endothelial cells (life extended by expression of the SV40 large T antigen) were added onto the denuded Descemet's membrane and allowed to attach in culture at 37 degree C. Evidence of corneal cell attachment to Descemet's membrane was determined between 1 and 8 h by scanning and transmission electron microscopy. Donor life-extended corneal endothelial cells were labeled with a fluorescent dye to allow tracking of the donor cells following seeding onto denuded Descemet's membrane. In four independent experiments, the Descemet's repopulated corneas were placed into syngeneic mice and evaluated for corneal clarity after 6 weeks. RESULTS: We could detect attachment of the life-extended murine CEC by scanning and transmission electron microscopy to denuded Descemet's membrane. The optimal time for adherence was 2 h and these repopulated corneas were used as donors in a murine model of penetrating keratoplasty. Of 20 mice evaluated after 6 weeks, 4 displayed corneal clarity, and fluorescent evaluation demonstrated that only the donor corneal endothelial cells were present. CONCLUSIONS: This experimental protocol establishes that "life-extended" MCEC can bind to Descemet's membrane ex vivo and form a distinct monolayer. The repopulated Descemet's membrane allowed us to directly test the hypothesis that cultured life-extended corneal endothelial cells are functional when reintroduced into an in vivo milieu and provides evidence that specific corneal endothelial cell transplantation may be a viable alternative to pentrating keratoplasty.

Animals↗

PubMed2000

Corneal ectasia detected after laser in situ keratomileusis for correction of less than -12 diopters of myopia.

We report 2 cases of corneal ectasia detected after laser in situ keratomileusis (LASIK) for the correction of less than -12.0 diopters (D) of myopia. Patients were evaluated before and after LASIK by corneal topography and pachymetry. After treatment, visual acuity temporarily improved but was followed by visual impairment, with corneal ectasia detected by topography. There may be a risk of corneal ectasia after LASIK in cases of myopia of less than -12.0 D. Despite thelow incidence, we recommend that LASIK be restricted to cases in which more than half the original corneal thickness and more than 250 microns of the stromal bed can be preserved. Careful examination, including preoperative serial topographic evaluation and measurement of posterior stromal thickness, should be performed to improve the quality and predictability of corneal refractive surgery.

Adult↗

PubMed2000

High-resolution transcript map of the region spanning D12S1629 and D12S312 at chromosome 12q13: triple A syndrome-linked region.

For those searching for human disease-causing genes, information on the position of genes with respect to genetic markers is essential. The physical map composed of ESTs and genetic markers provides the positional information of these markers as well as the starting point of gene identification in the form of genomic clones containing exons. To facilitate the effort of identification of genes in the region spanning D12S1629 and D12S312, we constructed a high-resolution transcript map with PAC/BAC/cosmid clones. The strategy for the construction of such a map involved utilization of STSs for the screening of the large insert bacterial chromosome libraries and a chromosome 12-specific cosmid library by hybridization. The contig was constructed based on the STS contents of the clones. The resulting high-resolution transcript map of the region between P273P14/SP6 and D12S312 spans 4.4 cM from 66.8 to 71.2 cM of the Généthon genetic map and represents approximately 2.4 Mb. It was composed of 81 BAC, 45 PAC, and 91 cosmid clones with a minimal tiling path consisting of 16 BAC and 4 PAC clones. These clones are being used to sequence this part of chromosome 12. We determined the order of 135 STSs including 74 genes and ESTs in the map. Among these, 115 STSs were unambiguously ordered, resulting in one ordered marker per 21 kb. The order of keratin type II locus genes was determined. This map would greatly enhance the positional cloning effort of the responsible genes for those diseases that are linked to this region, including male germ cell tumor as well as palmoplantar keratoderma, Bothnian-type, and triple A syndrome. This transcript map was localized at human chromosome 12q13.

Addison Disease↗

PubMed2000

Stimulation of quiescent corneal endothelial cells by direct delivery of the SV40 large T-antigen protein.

PURPOSE: To determine whether the delivery of the SV40 large T-antigen is a feasible method for transiently inducing proliferation of corneal endothelial cells. METHODS: Liposome-mediated delivery of proteins into bovine corneal endothelial cells (BCEC) was utilized in this study. Initially, beta-galactosidase was used as a marker protein for cell delivery and cells were assayed colorimetrically for beta-galactosidase activity. Subsequently, SV40 large T-antigen protein was introduced into BCEC and positive cells were identified by immunohistochemistry 24 hours after liposome-protein treatment. Quiescent BCECs were double-labeled using BrdU as a measure of de novo DNA synthesis and the SV40 large T-antigen was detected by standard immunohistochemical methods. RESULTS: Beta-galactosidase or SV40 large T antigen were introduced into BCECs using liposome transfer methods. The transfer efficiency of beta-galactosidase was > 30% of the cells. SV40 large T antigen was successfully introduced and was localized to the nuclei of BCECs. The treatment of quiescent BCECs with large T antigen caused an increase in BrdU incorporation. Co-labeling confirmed that only cells containing SV40 large T antigen were positive for de novo DNA synthesis. CONCLUSIONS: This study demonstrates that proteins can be inserted directly into corneal endothelial cells. In the case of the SV40 large T-antigen, the protein localized to the nucleus and maintained its bioactivity by inducing DNA synthesis. This finding suggests that liposome-mediated delivery of transforming proteins could be a method to transiently induce corneal endothelial cell proliferation.

Animals↗

PubMed2000

Overexpression of the transforming growth factor-beta-inducible gene betaig-h3 in anterior polar cataracts.

PURPOSE: In anterior polar cataracts and the fibrosis that can occur after cataract surgery, lens epithelial cells synthesize abundant extracellular matrix molecules and transdifferentiate into myofibroblast-like cells. Transforming growth factor (TGF)-beta has been implicated as a key player in these cataractous changes. The purpose of this study was to determine whether the TGF-beta-inducible gene h3 (betaig-h3) is expressed in lens epithelial cells from patients with anterior polar cataracts and to test whether betaig-h3 is induced by TGF-beta in cultured lens epithelial cells. METHODS: Lens epithelial cells attached to the anterior capsules of human cataractous lenses and noncataractous lenses were examined for the expression of betaig-h3 mRNA and protein using reverse transcription-polymerase chain reaction and immunohistochemical analyses. The effect of TGF-beta on betaig-h3 gene expression was also tested in human lens epithelial B-3 cells using Northern and Western blot analyses. RESULTS: betaig-h3 mRNA was not detected in lens epithelial cells from patients with clear lenses or patients with nuclear cataracts. Significant expression of mRNA for betaig-h3 was observed in lens epithelial cells from patients with anterior polar cataracts. Immunohistochemical analysis using anti-betaig-h3 antiserum indicated that betaig-h3 protein was present within the subcapsular plaques of anterior polar cataracts. Treatment of human lens epithelial B-3 cells with TGF-beta1 led to an increase in betaig-h3 mRNA and the secretion of betaig-h3 protein into the culture medium. CONCLUSIONS: betaig-h3 may serve as a marker for anterior polar cataracts in addition to previously known proteins, fibronectin, type I collagen, and alpha-smooth muscle actin. The functions of this protein in lens pathology need to be further investigated.

Animals↗

PubMed1999

Immunocytochemical localization of nitric oxide synthase in the mammalian retina.

The localization of nitric oxide synthase (NOS) was investigated by immunocytochemistry and immunoblotting using an antiserum against neuronal NOS in the rat, mouse, guinea pig, rabbit and cat retinae. Western blot analysis of retinal tissue extracts showed that the NOS-immunoreactive band of 155 kDa was present in all species. In the rat, mouse, guinea pig and rabbit retinae, two types of amacrine cells and a class of displaced amacrine cells were consistently NOS-labeled. In the cat retina, unlike other mammals, one type of amacrine cells and two types of displaced amacrine cells showed NOS immunoreactivity. NOS immunoreactivity was further found in some bipolar cells of the rat and guinea pig, some interplexiform cells of the mouse, some photoreceptor cells of the rabbit and some Müller cells of the cat.

Animals↗